ECG : Red Book Diagnoses

Cases from Red Book

Acute inferior MI
Old anteroseptal MI
Wolff-ParkinsonWhite Syndrome
Atrial flutter with
2:1 conduction
Atrial fibrillation
and LVH

Complete heart block

Pulmonary embolism
Wide complex
tachycardia
Supraventricular
tachycardia
Sinus bradycardia, RBBB,
sinus arrhythima and
prolonged QT interval

STEMI
Convex ST segment elevation over
Inferior leads: II, III, aVF
Lateral leads: I, aVL, V6
Anteriorseptal / lateral: V1-3, V4-6
Right ventricular: V3R, V4R (also by V1
and III>II changes)

Diagnosis: Acute ________

myocardial infarction

Hyperacute Anteroseptal
STEMI

Hyperacute Anteroseptal
STEMI

ST elevation: V1-4
Q waves: V1-2
Hyperacute T waves: V2-4
Additional STE in I, aVL, V5 and
reciprocal depression in lead III
Pathology: occlusion of the left
anterior descending artery (LAD)

Prior Anteroseptal MI

Prior Anteroseptal MI

Deep Q waves: V1-V3

Residual ST elevation: V1-V3
Biphasic / inverted T waves: V1-V5
Poor R progression: R < 3mm in V3

Extensive Anterior MI

Anterior-inferior STEMI (wraparound

LAD)

 Anterior STEMI LAD worst

prognosis
Investigations to help diagnosis: CXR,
cardiac enzyme, radionuclide
imaging, echocardiogram

Causes of Left Axis

Deviation

LVH
LBBB
Inferior MI
Ventricular pacing
WPW

Causes of Right Axis

Deviation

RVH
Acute RV strain (e.g. due to PE)
Lateral STEMI
COPD
Hyper K, Na channel blockade (TCA
poisoning)
Dextrocardia

Hyper K ECG changes

> 5.5
Peaking of T waves

> 6.5
Flattening of P waves
Lengthening of PR interval

> 7.0
High grade conduction block
Eventually arrest

Hyper K 7.0

Hyper K 9.0

Common P Wave
Abnormalities
P mitrale = bifid P waves seen in
left atrial enlargement
P pulmonale = peaked P waves
seen in right atrial enlargement
P inversion: ectopic atrial and
junctional rhythms
Variable P morphology: multifocal
atrial rhythms

Pathological Q waves

> 1mm wide

> 2mm deep
> 25% of QRS complex
Seen in V1-V3 (small septal Q in V5-V6 is normal)

Current or prior myocardial infarction (persists

indefinitely in 85%)
Persistent ST elevation + Q wave => ventricular
aneurysm
Isoelectric ST segment = non-acute (months to
years)

Abnormal Q waves in
Wolff-Parkinson-White syndrome
Pseudo-infarction pattern in in 70%
Negative delta waves => Pseudo-Q
waves

LBBB
COPD
HOCM: septal hypertrophy
Pulmonary embolism: S1Q3T3

Investigations for old MI

CXR
Cardiac enzyme
Echocardiogram
Radionuclide imaging
Cardiac catheterization
MRI imaging

Delta Wave

Wolff-Parkinson-White
syndrome
Short PR interval < 120 ms
Wide ORS complex > 100 ms
Slurred upstroke to QRS complex i.e. the
delta wave
+/- secondary ST and T changes
Can lead to: atrial fibrillation, ventricular
fibrillation, paroxysmal supraventricular
tachycardia

Atrial Fibrillation in WPW

Rate > 200 bpm, irregular rhythm,
wide QRS (accessory pathway), QRS
change in morphology, stable axis
Treatment by nodal blocking is
CONTRAINDICATED; give
procainamide or amiodarone instead
If unstable, DC cardioversion

Atrial Flutter
Narrow complex tachycardia at 150
bpm
Narrow complex tachycardia
Flutter waves in inferior leads
(inverted flutter waves =
anticlockwise = commonest)
Vagal manoeuvres: increases block,
unmask flutter waves (but doesnt
terminate)

Atrial Fibrillation
Atrial rate = 400 600 bpm
P waves are absent
Ventricular rate is irregularly irregular

Irregularly irregular
Atrial fibrillation
Multifocal atrial tachycardia
Atrial rate > 100
More than 3 P morphologies
PR, RR, RP intervals vary

Atrial flutter or atrial tachycardia with

variable block

Investigation and Symptomatic Mx

of Atrial Flutter and Atrial Fibrillation
Investigations
CXR
Electrolytes
Cardiac enzymes
Thyroid function test
Echocardiogram

Rate and symptom control

Digoxin, diltiazem, verapamil, betablockers and amioderone

Left ventricular hypertrophy

Voltage criteria
Sokolov-Lyon criteria: SV1 + RV5/6 > 35
mm
Any R+S > 45 mm

Non-voltage criteria
ST segment depression
Asymmetrical T inversion (LV strain
pattern)

Causes of LVH

Hypertension
AS
AR
MR
Coarctation of the aorta
HOCM

Causes of ST depression and T

inversion
Digoxin toxicity
Can lead to complete heart block
Classical cause of junctional tachycardia
(= junctional rhythm > 100 bpm, narrow
complex, retrograde P waves)
Exacerbated by hypo K, Mg an Ca

MI

AV Block
First degree
PR > 200 ms
In marked first degree block, PR > 300
ms and P waves are buried in preceding
T wave

Causes of 1 degree block

st

Increased vagal tone

Athletic training
Inferior MI
Hypokalaemia
Post cardiac surgery
AV nodal blocking agents (betablockers, CCB, digoxin, amiodarone)

AV Block
Second degree
Mobitz I or Wenckebach phenomenon:
progressive prolongation of PR interval
culminating in a non-conducted P wave
Mobitz II: intermittent non-conduction
without progressive prolongation of PR
interval

Mobitz I vs Mobitz II
Mobitz I is due to functional suppression
of AV conduction, whereas Mobitz II is due
to structural damage to the conducting
system
Mobitz II causes
Anterior MI
Idiopathic fibrosis of conducting system (Levs
disease)
Autoimmune causes
Infiltrative myocardial disease

Complete Heart Block

Complete absence of AV conduction
Perfusing rhythm is a junctional or
ventricular escape
Characteristics: bradycardia, AV
dissociation (constant PP and RR but
variable PR)

Potentially reversible causes of

complete heart block

Hyperkalaemia
Endocarditis
Acute myocardial infarction
Digoxin toxicity
Lyme disease

Acute Pulmonary Embolism

Sinus tachycardia, S1Q3Tinv3
Other changes
Frontal plane lead changes that mimic acute
interior MI
RAD, RBBB

Diagnostic tests
CXR
CT thorax
Ventilation-perfusion scan
Pulmonary angiogram

Wide Complex Tachycardia

Causes
VT
SVT + RBBB
SVT + aberrant conduction
Antidromic tachycardia + accessory pathway

Investigations
CXR, electrolytes, cardiac enzymes,
echocardiogram

External DC cardioversion

QRS features suggestive of

VT

AV dissociation
Capture, fusion
> 140 ms for RBBB and > 160 ms for LBBB
Precordial deflection concordance
R > R in V1 (in RBBB, right rabbit ear is
taller)

Discordance, aberrantly conducted atrial

premature beats and QRS morphology similar
to sinus rhythm suggests aberrancy

Supraventricular
tachycardia
Features
Narrow complex tachycardia
Retrograde atrial activation (II, III, aVF)
ST/T abnormalities (ischaemia)

Causes of SVT
AV nodal re-entry tachycardia (P fused
to QRS)
AV re-entry tachycardia (P in ST)
Atrial tachycardia (R > QRS)

Investigation and Management of

SVT
Ix
CXR
Electrolytes
Cardiac enzymes
Thyroid function test

Immediate treatment
Vagal meneuvers, adenosine, verapamil
(fast-acting nodal blocking)

Causes of prolonged QT interval

Drugs: antiarrhythmics, antibiotics
(erythromycin, clarithromycin),
antihistamine (terfenedine,
diphehydramine) and anti-psychotics
Electrolytes: hypo K, Ca and Mg
Congenital: long QT syndromes
Metabolic: hypothyroidism and
diabetes
Vascular: stroke, SAH, IHD

RBBB
Features
QRS > 120 ms
RSR in V1 (M-pattern), DDx Brugada
syndrome
Wide slurred S wave in V5-V6 (W-pattern)
Can occur in normal subjects

In LBBB, there is W V1 and M V6;

causes include AS, IHD, HT, dilated
cardiomyopathy, MI